BACKGROUND:Pathologic staging and grading are the most important prognostic factors in prostatic cancer. Unfortunately, pathologic staging needs to be evaluated by surgical procedures; moreover, the proposed grading systems are largely based upon subjective histopathologic evaluations. In recent years, these problems have been approached with flow cytometry (FCM). The present study evaluates the significance of DNA ploidy of prostatic carcinoma assessed by FCM.MATERIALS AND METHODS:Microscopic slides from 132 core needle biopsies and 22 surgical specimens of prostatic carcinoma were reviewed and classified according to Gleason's score modified by Epstein et al. Formalin-fixed, paraffin-embedded tissue samples were prepared for FCM evaluation using standard techniques. Adequate histograms were obtained from 113 biopsies (85.6%) and from all the surgical specimens (100%).RESULTS:Among the 113 biopsy specimens, a statistically significant correlation was found between DNA ploidy and Epstein's grading, since high-grade neoplasms accounted for 40.38% of non-diploid cases and only for 21.33% of diploid cases (chi square = 5.8; p = 0.05). Moreover, tetraploid tumors were defined as a separate FCM category with an absolute prevalence (65.52%) of non-high grade neoplasms (chi square = 5.9; p = 0.05). Although not submitted to statistical analysis, data collected from surgical specimens showed similar distribution.CONCLUSIONS:DNA ploidy assessment by FCM is a viable procedure in the majority of needle biopsy tissue samples of prostatic carcinoma; it may produce prognostic parameters with greater objectivity than conventional histologic grading.

The p53 tumour suppressor gene has an important role in the the maintenance of genome stability and its mutational inactivation may be at the origin of aneuploidy in cancer cells. The aim of this study was to determine whether p53 mutations were associated to DNA aneuploidy, as assessed by flow cytometry, in colorectal adenocarcinomas. Analysis of p53 mutations spectrum of the sorted nuclei was done by Denaturing Gradient Gel Electrophoresis (DGGE) and DNA sequencing. Overall, we studied 20 adenocarcinomas, the corresponding control mucosa, and 7 lymph node metastases. Five tumours (25%) were DNA diploid, while 15 tumours (75%) were composed of DNA aneuploid and diploid subpopulations. DNA diploid control mucosa and adenocarcinomas showed no p53 mutations, while 60% of the tumours with DNA aneuploidy had p53 mutations. Therefore, p53 mutations occurred significantly more often in DNA aneuploid than in DNA diploid tumours (p < 0.04, Fisher’s exact test). Incidences of DNA aneuploidy and p53 mutations in lymph node metastases were 60 and 86%, respectively. In all tumours showing a p53 mutation, the wild-type allele was not or only bearly visible in DNA aneuploid cells suggesting that, in such cells, aneuploidy is accompanied by complete p53 functional inactivation. The present observations suggest that p53 mutations may have a role in the origin of aneuploidy at late stages of colorectal carcinogenesis.